Nakada T
Urol Int. 1984;39(1):40-5. doi: 10.1159/000280942.
Following 7 days on a low sodium diet, a regular sodium diet or a high sodium diet each, urine samples were collected from 37 subjects in the final days of each sodium treatment. Urinary kallikrein excretion was determined in 9 patients with primary aldosteronism, 15 normal subjects and 13 patients with essential hypertension. Urinary aldosterone excretion, plasma renin activity (PRA), urinary sodium excretion, urinary potassium excretion and p-aminohippuric acid clearance were also determined on the same days. Levels of urinary kallikrein excretion in patients with primary aldosteronism due to aldosterone-producing adenoma (APA) were greater (p less than 0.05 to p less than 0.001) than those in patients with primary aldosteronism due to idiopathic adrenal hyperplasia (IHA) under any sodium diet. Other examined variables were of limited value in differentiating patients with APA from those with IHA. Urinary kallikrein excretion, urinary excretion of electrolyte, urinary aldosterone excretion, PRA and PAH clearance were similar in normal subjects and patients with essential hypertension. It appears reasonable to conclude from these data that urinary kallikrein does not play an important role in the pathogenesis of essential hypertension, and elevated urinary kallikrein excretion in patients with primary aldosteronism due to APA can be used for biochemical differentiation from those with IHA.
在分别采用低钠饮食、常规钠饮食或高钠饮食7天后，在每种钠治疗的最后几天从37名受试者中收集尿样。测定了9例原发性醛固酮增多症患者、15名正常受试者和13例原发性高血压患者的尿激肽释放酶排泄量。在同一天还测定了尿醛固酮排泄量、血浆肾素活性（PRA）、尿钠排泄量、尿钾排泄量和对氨基马尿酸清除率。在任何钠饮食条件下，由醛固酮分泌腺瘤（APA）引起的原发性醛固酮增多症患者的尿激肽释放酶排泄水平均高于由特发性肾上腺增生（IHA）引起的原发性醛固酮增多症患者（p小于0.05至p小于0.001）。其他检测变量在区分APA患者和IHA患者方面价值有限。正常受试者和原发性高血压患者的尿激肽释放酶排泄、电解质尿排泄、尿醛固酮排泄、PRA和PAH清除率相似。从这些数据可以合理地得出结论，尿激肽释放酶在原发性高血压的发病机制中不发挥重要作用，并且由APA引起的原发性醛固酮增多症患者尿激肽释放酶排泄升高可用于与IHA患者进行生化鉴别。
